Mechanisms on Boron-Induced Alleviation of Aluminum-Toxicity in Citrus grandis Seedlings at a Transcriptional Level Revealed by cDNA-AFLP Analysis

The physiological and biochemical mechanisms on boron (B)-induced alleviation of aluminum (B)-toxicity in plants have been examined in some details, but our understanding of the molecular mechanisms underlying these processes is very limited. In this study, we first used the cDNA-AFLP to investigate the gene expression patterns in Citrus grandis roots responsive to B and Al interactions, and isolated 100 differentially expressed genes. Results showed that genes related to detoxification of reactive oxygen species (ROS) and aldehydes (i.e., glutathione S-transferase zeta class-like isoform X1, thioredoxin M-type 4, and 2-alkenal reductase (NADP+-dependent)-like), metabolism (i.e., carboxylesterases and lecithin-cholesterol acyltransferase-like 4-like, nicotianamine aminotransferase A-like isoform X3, thiosulfate sulfurtransferase 18-like isoform X1, and FNR, root isozyme 2), cell transport (i.e., non-specific lipid-transfer protein-like protein At2g13820-like and major facilitator superfamily protein), Ca signal and hormone (i.e., calcium-binding protein CML19-like and IAA-amino acid hydrolase ILR1-like 4-like), gene regulation (i.e., Gag-pol polyprotein) and cell wall modification (i.e., glycosyl hydrolase family 10 protein) might play a role in B-induced alleviation of Al-toxicity. Our results are useful not only for our understanding of molecular processes associated with B-induced alleviation of Al-toxicity, but also for obtaining key molecular genes to enhance Al-tolerance of plants in the future.

硼（B）诱导缓解植物铝（Al）毒性的生理生化机制已有较为细致的研究，但目前学界对该过程背后的分子机制仍知之甚少。本研究首先采用cDNA扩增片段长度多态性（cDNA-AFLP）技术，分析了柚（Citrus grandis）根系响应硼与铝交互作用的基因表达模式，并筛选得到100个差异表达基因。结果显示，与活性氧（ROS）和醛类解毒相关的基因（如谷胱甘肽S-转移酶ζ类样同工型X1、硫氧还蛋白M型4、2-烯醛还原酶（NADP+依赖性）类似物）、代谢相关基因（如羧酸酯酶、卵磷脂-胆固醇酰基转移酶样4样、烟碱胺氨基转移酶A样同工型X3、硫代硫酸硫转移酶18样同工型X1、铁氧还蛋白NADP+还原酶（FNR）根系同工型2）、细胞运输相关基因（如非特异性脂质转移蛋白样蛋白At2g13820样、主要促进因子超家族蛋白）、钙信号与激素相关基因（如钙结合蛋白CML19样、吲哚-3-乙酸-氨基酸水解酶ILR1样4样）、基因调控相关基因（如Gag-pol多蛋白）以及细胞壁修饰相关基因（如糖基水解酶家族10蛋白），可能在硼诱导缓解铝毒性的过程中发挥作用。本研究结果不仅有助于我们理解硼诱导缓解铝毒性的分子过程，同时也为未来挖掘可用于提升植物铝耐受性的关键功能基因提供了重要参考。